GI Flashcards
1
Q
SMA syndrome
- what happens
- sxs
- worse
- improve
A
- duodenum compressed by SMA
- stomach pain
- eating
- left lateral recumbent
2
Q
Obstruction of duodenum
- how to fix
A
- re-route GI tract so food can bypass blockage
3
Q
IMA
- supplies
- gives off
A
- distal part of transverse colon, descending, sigmoid,
- inferior rectal a
4
Q
SMA
- supplies
- great colic artery
- ileocolic artery
A
- lower duodenum, small intestine, ascending colon, and prox 2/3 colon
- ascending colon
- ileum and cecum
5
Q
What is first part of GI to be affect with hypotension
A
- splenic flexure, only gets some flow from IMA and SMA
6
Q
marginal a of drummen
A
- sits against wall of intestine
7
Q
arc of riolan
A
runs in mesentary, communicates between IMA and SMA
8
Q
Blood supply to liver
- artery
- runs w
- pringle manuever: what is it, what does it mean
- triad anatomy
- venous
A
- proper hepatic
- portal v and bile duct
- clamp duct, a, v when there is bleed in liver -> if continue to bleed then it is venous
- ant: bile duct, artery, portal v
- right, middle, and left hepatic v -> dump into vena cava
9
Q
Embryology
- starts as
- leaves
- returns
- turns
- foregut: includes, a, PS, S, lungs
- migut: includes, a, PS, S, rotation
- hindgut: includes, a, PS, S
A
- straight tube
- abd cavity through umbilicus at 6 weeks
- abd cavity at 10 weeks
- 270 degress counterclockwise
- esophagus, stomach, liver gall, upper duodenum -> Celiac trunk, PS- Vagus, S: splanchnic; gives rise to lung buds
- lower duodenum, small intestine, ascending colon, and prox 2/3 colon -> SMA, PS - vagus, S: splanchnic; rotation requires cilia and if have dyskinesia then will have all organs on opp side
- distal 1/3 of transverse colon, descending colon, sigmoid colon -> IMA, PS: pelvic splanchnic, S: lumbar splanchnic
10
Q
- malrotation: cecum, midgut, sxs; worst case scenario; tx
A
- cecum is in RUQ and held in place by ladds bands; midgut fixed to SMA; newborn baby in first few days of lay has bilious vomitting; malrotation causes necrosis and gangrene of intestines; surgery -> remove bands, remove necrotic tissue -> put everything back in place (cecum will end up in LUQ, so remove appendix)
11
Q
acute mesenteric ischemia
- sxs
- palpation
A
- pt in excutiating pain but do not see much on PE, signs of sepsis
- doughy on palpation
12
Q
Anus
- upper: contains, mucosa histo, connects to lower w, blood supply
- lower: histo, blood supply
- hiltons white line: what is it
- dentate line: what is it and why is it important
A
- longitudinal folds/ elevations of mucosa; simple columnar epi; connectes w/ anal valves; sup rectal
- stratified squamous epi; inferior rectal
- junction between keratinized stratified squamous epithelium and non-keratinized stratified squamous epi
- above is rectum w/ columnar epi (colorectal CA) and visceral innervation (painless); anus w/ squamous epi (squmous cell CA) and painful
13
Q
Retroperitoneal stuctures
- solid
- hollow
- vessels
- SAD pucker
- cause of retroperitoneal hematoma in stable pt
A
- pancreas, kidney, adrenal
- part 2-3 of duodenum, ascending and descending colon, rectum, ureters, bladder
- abd aorta, inferior vena cava
- pancreatic injury w/ venous bleeding
14
Q
Tongue
- taste
- Pain
- motor
- ant 2/3 tongue
- post 1/3 tongue
- taste
A
- 7, 9, 10
- 3, 9, 10
- 12
- 1st branchial arch; tast from chorda tympani of CN7, sensation from madibular division of 5
- 3rd and 4th branchial arches; tase and sensation from CN 9
- inside taste bud is gustatory cell which has gustatory hair which detects chemical compound you are injesting, activate sensory fibers and they take info to brain
15
Q
Oral gland innervation
- PS
- Symp
- parotid
- lingual
- sublingual
- submandibular
A
- increase secretion
- decrease secretion
- serous -> CN9
serous -> CN7 - mucinous -> CN7; under tongue
- mucinous -> CN7; under jaw
16
Q
Saliva
- 1st step in
- rich in
- lipase
- amylase
- lysozyme
- HCO3
A
- digestive process
- IgA
- break down fat
- begins carb breakdown; bacteria in mouth break down carb -> produce lactic acid -> destroy enamel -> lead to dental carries
- detergent that binds and reoves things from teeth that get stuck near mucinous secreting glands
- protect teeth and gum from acid erosion from food, frinks, and reflux
17
Q
Cleft lip
- what is it
- when does it develop
- what happens
- caused by
A
- failure of fusion of maxillary and medial nasal process
- week 5
- under dev of of mesenchyme of maxillary swelling causing inadequate contact w/ medial nasal process and intermax process
- anti-seizure, vit A
18
Q
Cleft palate
- develops
- caused by
- tx
A
- 8 weeks - 12 weeks
- lat palantine process, nasal septum and/ or median palantine process
- in US fixed immediately but in other countries w/o resources will have to wait till older sometimes even adult hood
19
Q
Swallowing
- process
A
- chew food and mix with saliva to form paste -> tongue pushes bolus into post oral pharynx -> soft palate elevates to close nasopharynx -> larynx blocks trachea so you dont aspirate -> bolus goes down esophagus
20
Q
Muscles of tongue
- mylohyoid
- genioglossi
- styloglossus
- hyoglossus
- palatoglossus
A
- tongue elevation
- tongue protrusion
- trough formation
- tongue depression and retraction
- elevates post tongue and closes oropharyngeal isthmus; innervated by vagus
21
Q
Odynophagia
- what is it
- bugs
- healthy person causes
A
- painful swallowing
- candida or CMV (cowdry bodies)
- pill swallowing
22
Q
Dysphagia
- what is it
- progressive worsening
- chronic
- paradoxical
- cardiovascular
A
- difficulty swallowing
- stop solids first, then soft food, then liquids; cancer
- achalasia ->
- only with liquid
- dilated left atrium pushing on esophagus; will have mumur and rales with pain
23
Q
Dysphagia
- what is it
- progressive worsening
- chronic
- paradoxical
- cardiovascular
A
- difficulty swallowing
- stop solids first, then soft food, then liquids; cancer
- achalasia -> LES fails to open up during swallowing
- only with liquid
- dilated left atrium pushing on esophagus; will have mumur and rales with pain
24
Q
Achalasia
- what happens
- caused by
- bug
- dysphagia types
- barium swallow
- increased risk of
- mgmnt
A
- LES fails to open up during swallowing
- auerbach/ myenteris plexus -> unopposed PS causing contraction of LES
- chagas dx -> destroys myenteric plexus
- chronic and paradoxical
- bird beak
- esophageal CA
- Ca channel blocker and Nitrates -> SM relax (GERD), botox which causes paralysis of muscle 4-6 months of relief, mechanical dilation
25
Q
Barrets Esophagus
- what is it
- caused by
- common cause
- management
A
- metaplasia of squamous epi to columnar epi
- chronic gastric acid exposure
- hiatal hernia -> increase in GERD (only 6% chance)
- should be scoped and biopsied every year to monitor for CA
26
Q
CA of esophagus
- squamous: risk, location
- adeno: common,risk, location
- sxs
A
- smoking and EtOH, prox; flattened polyhedral or ovoid elpi with eosinophilic cytoplasm, keratin pearls of whirls; esophageal resection (either pull stomach into chest to attach or take part of colon and put it as a link between stomach and esophagus
- most common; barrets, distal;
- weight loss, dysphagia
27
Q
Mallory Weiss tear
- what is it
- caused by
- bleeding time
- sxs
- diff from varices
A
- longitudinal tear of mucosa at gastro-esoph junction
- reching, coughing, vomitting
- EtOH use of eating disorder
- stop abruptly in 24-48 hrs
- blood in mouth or melena
- will vomit bucket of bloods vs only a bit of blood
28
Q
boerhaave syndrome:
- what is it,
- hammans sign ,
- pleural fluid tap;
- tx
A
- esophageal rupture,
- usually iatrogenic,
- crunch in precordium that is synchronous with heartbeat;
- amylase, lipase, w/ contents from saliva
- drain and resect/ or tie off and give them a feeding tube directly into stomach
29
Q
zenkers diverticulum
- what is it
- caused by
- sxs
- sequeleae
- diff from traction
A
- false diverticulum that sits about UES
- congenital or excessive pressure (problem with synchronized contraction, upper and lower muscles squeeze at same time causing increase and pressure and an outpuching)
- dysphagia, halitosis (food get stuck in out pouching), or asymptomatic
- problem with synchronized contraction -> peristalsis
- inflamm process causes adhesion and the diverticulum is caused by pulling and is true vs zenckers is pushed out bc of pressure and it is false
30
Q
Plummer vinson syndrome
- triad of findings
- location
- increase risk of
- management
A
- dyphagia (to solids), esophageal webs, iron def anemia
- proximal
- squamous cell CA
- teat anemia, modify diet to make pt comfortable, only resect rings w/ severe odynophagia
31
Q
Schatzki ring
- location
- sxs
- management
A
- web in lower esophagus
- intermittent dysphagia, and felling of food sticking when swallowing
- modify diet
32
Q
Diffuse esophageal spasm
- what is it
- sxs
- triggered
- imaging
- tx
A
- uncoordinated contraction of whole esophageal body (LES remains intact)
- dysphagia, regurg, severe CP (mimics MI)
- very hot or cold beverages
- corkscrew
- CCB, nitate -> relax muscles, botox or surgical balloon dilation
33
Q
tracheo-esophageal ridges
- when
- sxs
- imaging
- H configuration
- type C
A
- failure of fusion of tracheoesophageal ridges during 3rd week of embryogenesis
- on very first feeding baby will vommit of choke
- see blind pouch and air in stomach if trachea is attached to stomach
- esophagus attached to stomach and trachea; no vomitting but every feed child will aspirate
- most common; prox esophagus ends in blind pouch and lower is attached to stomach and trachea
34
Q
GERD
- what is it
- associated w
- sxs
- increased risk of
- DX
A
- abnormal relax of LES allows stomach contents/acids to move into lower esophagus
- hiatal hernia
- heart burn, cough (if acid comes into pharynx), erosion of dental enamel, laryngitis, pharyngitis
- barrets
- pH probe, also known as esophageal manometry
35
Q
Esophageal Varices
- what is it
- MCC
- route
- dx
- tx
A
- overly dilated v in lower esophagus
- portal HTN secondary to cirrhosis
- Portal vein -> left gastric v -> superficial esophageal v
- endoscopy
- ligate, band or inject them if not bleeding and cauterize or tamponade (with balloon) if bleeding
36
Q
Anatomy of Stomach
- orad: where,
- caudal: where
A
- middle of body and up; much thinner muscular wall than distal part; higher risk of perforation
- middle of body and down; rugae are larger and thicker musclar walls; churning
37
Q
Function of Stomach
- protein digestion
- vit B 12
- gastric resevoir
A
- occurs mainly in stomach via parietal cells producing HCL and chief cells producing pepsinogen (converted to pepsin with low pH)
- parietal cells secrete intrinsic factor to allow absorption in terminal ileum; with gastrectomy will have lifelong B12 supplementation
- holds food while partitions small amounts to go through small intestine so digestion can occur properly
38
Q
Acid secretion
- celiac phase: mediated by; triggered by
- gastric phase: mediated by; triggered by
- intestinal phase
A
- mediated by PS; thought/ site/ taste of food causes production of gastric acid
- mediated by presence of gastrin; chemical stimulus of food and distention of stomach
- when protein contains food enters duodenum
39
Q
- mucous cell: prduce, in response to
- parietal
- chief
- G cells
- interchromafin cells
- D cells
A
- mucus and biarb bc of prostaglandin
- HCl
- pepsinogen
- gastrin
- histamine -> increase secretion of acid
- somatostatin -> inhibits secretion of acid and peristalsis
40
Q
Receptive Relaxation
- what is it
- how does it work
- VIP
A
- allows stomach to relax in orad region to allow more room for food
- detect stretch -> send afferent through vagus to brain and efferent through vagus to stomach releasing VIP
- SM relaxation
41
Q
Gastric emptying
- time frame
- why is it reg
- slows down bc
- CCK
- why acid
A
- 3 hour
- allow neutralization of stomach acid duodenum and optimal absorption
- Acid (myenteric plexus) and fat (CCK)
- causes gallbladder to contract so bile can enter into duodenum so fat can be broken down into smaller globules and lipase has more SA to breakdown fat
- acid must be neutralized in order to get more food into duodenum
42
Q
How is acid produced
- histamine
- gastrin
- Ach
A
- binds H2 receptor on parietal
- produced by g cells, binds to parietal cell; also causes release of pepsinogen
- from vagus; can cut branches of vagus nerve that go to parietal cells
43
Q
Dumping Syndrome
- what is it
- sequelae
- sxs
A
- connect duodenum to esophagus
- no longer have pylorus to partition off amount of food in stomach so now have hyper osmotic in lumen causing water to be dumped into intestine
- hypovolemia, hypoglycemia (all glucose dumped into duodenum causes lots of insulin to be released), diarrhea, flushing, bloating
44
Q
Gastrinoma
- what is it
- location
- produces
- sxs
- other tests
- managment
A
- neuroendocrine tumors, benign lesion
- pancreas, between pancreas and duodenum, 2nd part of doudoneum
- gastrin -> no feedback -> excessive acid production
- ulcers in weird places (NOT in stomach or in 1st portion of duodenum), diarrhea,
- MEN1 (PTH)
- PPI and removal if good candidate
45
Q
Protecting stomach
- what
- stimulated by
- other mech
A
- mucus
- prostaglandin -> from AA
- HCO3 -> neutralizes
46
Q
Parietal Cells - release - location - histo -
A
- HCl (H/ K on apical side) and IF
body and fundus - eosinophilic sytoplasm, increased mito and internal tubulovesicular sxs
- Ach on M3, Histamine on H2, and gastrin on gastrin receptor
47
Q
Tx of acid production
- antacid
- milk alkali
- H2 blockers
- PPI: MOA, benefit, AE, azole
A
- mostly use CaCO3
- drink milk and take a lot of antacids -> overwhelming body w/ Ca
- only drop by 70%; ranitidine, cimetidine; antisedative, gynecomastia
- stops production of acid -> 0 acid production occurs; omeprazole and pantoprazole; Ca issues bc no neg feeback from gastrin and it stimulates PTH and also decreases amount of Ca being absorbed; cannot give azole with it bc they need acidic pH to be activated
48
Q
Systemic mastocytosis
- what is it
- sequelae
A
- prolierfastion of mast cells in BM and other organs causing deposition of nest of mast cells in mucosa
- produces histamine causing immune reaction; looks like allergic reaction -> will cause hyper-secretion of gastric acid
49
Q
Zollinger Ellison syndrome
- what is it
- leads to
A
- when excess gastrin is secreted by tumor
- ulcers in weird area or ulcer dx that needs to be given really high dose in order to control
50
Q
Erosion
- what is it
- vs ulcer
A
- superficial defects that do not go beyond mucosa
- defects through submucosa and can get into muscularis and through serosa to perforate
51
Q
H. pylori
- damages
- tx
- types of AB
A
- mucous layer making acid pass through epi cells
- 2 antibiotics, anti-secretory agent (PPI or H2b blocker) and bismuth (decrease adherence to mucousal cells and damage bacterial cell wall)
- amox, carithromycin, metro, tetracycline
52
Q
Diarrhea
- common causes
- osmotic
- secretory
- toxin
- viral-bacterial
- chronic
A
- infection, toxins, drugs
- too much in lumen causing water to be secreted to normalize - > will stop if pt stops eating
- something causing enterocyte to secrete water
- self limited
- transient but clears faster with antibiotics if bug is found
- 3 or more lose stools per day for 3- 4 weeks; lactase def, malabsorption, lax abuse, IBS
53
Q
Constipation
- first thought should be
- other causes
- idiopathic tx
A
- drugs (pain meds, iron)
- neurogenic (SC injury, spinabifida), endocrinpathy (DM), IBS
- bulk forming lax, dietary mod, increase fluid
54
Q
Gastritis
- type a
- type b
- causes
- acute caused by
- chronic: a, b, ab, chemical
A
- body
- antrum
- upper GI bleeds in children, teens, adults
- h. pylori, other infections
- a- AI, b- h. pylori, AB - environmental, chemical - reflux
